Renal Function: MRI's, eGFR, and other 'New' News

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Renal Function MRI's, eGFR, and other 'New' News

• Keelyn Ericson, MD
• April 24th, 2008

2
Overview

• MRI Contrast Agents Nephrogenic Systemic
  Fibrosis.
• Hypertension New treatment options.
• Sodium Bicarbonate Radiocontrast nephropathy
  made worse?
• eGFR When and how to use it.

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Warning
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MRI
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MRI Contrast Agents

• Nephrogenic Systemic Fibrosis.

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Nephrogenic fibrosing dermopathy

• Probably more properly referred to as Nephrogenic
  Systemic Fibrosis
• From Galan, Cowper, et.al.
• Nephrogenic systemic fibrosis (NSF) is a
  recently identified fibrosing disorder seen only
  in patients with kidney failure. It is
  characterized by two primary features
• Thickening and hardening of the skin overlying
  the extremities and trunk
• Marked expansion and fibrosis of the dermis in
  association with CD34-positive fibrocytes.

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Nephrogenic fibrosing dermopathy
Huh?

• What the heck is this?

How does it occur?
Who is at risk?
Is it serious?
Who needs to know about it?
Is there a treatment for it?
What are the options?
Review
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Nephrogenic fibrosing dermopathyHuh?

• Nephro- Greek ?ef??? (nephros) - kidney
• -genic Greek ?e??? (genes) born
• Fibrosing Latin fibrae (fiber)
  fiberforming
• Dermo- Greek d??µa (derma) skin, hide
• -pathy Greek p???? (pathos) passion,
  suffering, or (more commonly) disease

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Nephrogenic fibrosing dermopathyHuh?

• Nephro- Greek ?ef??? (nephros) - kidney
• -genic Greek ?e??? (genes) born
• Fibrosing Latin fibrae (fiber)
  fiberforming
• Dermo- Greek d??µa (derma) - "skin, hide
• -pathy Greek p???? (pathos) passion,
  suffering, or (more commonly) disease
• Kidney-born Fiber-forming Skin-disease
• AKA Nephrogenic Systemic Fibrosis
• Kidney-born Systemic
  Fiber-forming-state

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Nephrogenic fibrosing dermopathy
Huh?

• What the heck is this?

How does it occur?
Who is at risk?
Is it serious?
Who needs to know about it?
Is there a treatment for it?
What are the options?
Review
13
What the heck is this?

• It can make you look like this!

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What the heck is this?

• Seriously

The typical course begins with subacute swelling
of distal parts of the extremities and is
followed in subsequent weeks by severe skin
induration and sometimes anatomic extension to
involve thighs, antebrachium, and lower abdomen.
The skin induration may be aggressive and
associated with constant pain, muscle
restlessness, and loss of skin flexibility.
6 (All photos 10)
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What the heck is this?
In some cases, NSF leads to serious physical
disability, including wheelchair requirement. NSF
initially was observed in and thought to affect
solely the skin (thus the initial term
nephrogenic fibrosing dermopathy), but
more recent patient reports have demonstrated
that several organs may be involved. 6
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What the heck is this?
Yellow asymptomatic scleral plaques are common.
(They dont affect vision.)
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What the heck is this?
Fibrotic forearm skin.
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Nephrogenic fibrosing dermopathy
Huh?

• What the heck is this?

How does it occur?
Who is at risk?
Is it serious?
Who needs to know about it?
Is there a treatment for it?
What are the options?
Review
20
How does it occur?

• Etiology and Pathogenesis
• The disease did not exist prior to 1997
• How do we know?

21
How does it occur?

• Etiology and Pathogenesis
• The disease did not exist prior to 1997
• How do we know?
• Prior tissue samples (skin biopsies) have been
  reviewed no cases were found similar to samples
  identified for NSF since 1997.

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How does it occur?

• Etiology and Pathogenesis
• The disease did not exist prior to 1997
• The disease has only been found in patients with
  renal disease
• How do we know?

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How does it occur?

• Etiology and Pathogenesis
• The disease did not exist prior to 1997
• The disease has only been found in patients with
  renal disease
• How do we know?
• Of approximately 300 cases identified through
  2008, none have come from patients with normal
  renal function

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How does it occur?

• Etiology and Pathogenesis
• The disease did not exist prior to 1997
• The disease has only been found in patients with
  renal disease
• Multiple associations have been identified the
  most common, by far, has been with the
  administration of Gadolinium contrast agents
• But does that mean anything?

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How does it occur?

• Etiology and Pathogenesis
• The disease did not exist prior to 1997
• The disease has only been found in patients with
  renal disease
• Multiple associations have been identified the
  most common, by far, has been with the
  administration of Gadolinium contrast agents
• But does that mean anything?
• We think so

26
How does it occur?
Gd deposited in vessel walls of the skin
27
How does it occur?

• Sodium, Phosphate, and Calcium are found in
  vessel walls along with Gd many ESRD (dialysis)
  patients and Chronic Kidney Disease patients
  already have Ca/Phos metabolism disease (known
  commonly as secondary hyperparathyroid disease).

28
How does it occur?

• This is thought to lead to activation of some
  kind of fibrotic or scarring factor.
• Abnormal activation of fibrocytes is consistent
  with one theory of the pathogenesis of NSF.

29
How does it occur?

• I thought Gadolinium was fairly safe.

30
How does it occur?

• I thought Gadolinium was fairly safe.
• Gd-DTPA (Gd-Diethylene triamine pentaacetic acid
  or gadodiamide) was introduced in 1988 as a
  paramagnetic contrast agent for use in MRI scans
  and was believed to be safe for patients with
  impaired renal function. Free Gd ions can form
  precipitates with anions, such as phosphate,
  because of its poor solubility, and it is
  considered highly toxic in its ionic form.
  Marckmann et al have posited that NFD may result
  from liberated Gd ions deposited in the tissues.
  These molecules are known to be extremely toxic
  and to produce deposits of Gd with calcium
  phosphates in the tissues of rodents.

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How does it occur?

• English please

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How does it occur?

• English please
• Renal failure Gadolinium NSF
• (High risk)
• Renal failure Other stuff NSF
• (Perhaps)
• Gadolinium Other stuff NSF
• (Never)
• Renal failure Gadolinium Other stuff
  NSF
• (High risk)

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(Other Stuff)

• Vascular manipulation
• High dose Epo/Aranesp
• Clotting events
• Underlying clotting abnormalities
  (hypercoagulable states)

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Nephrogenic fibrosing dermopathy
Huh?

• What the heck is this?

How does it occur?
Who is at risk?
Is it serious?
Who needs to know about it?
Is there a treatment for it?
What are the options?
Review
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Who is at risk?

• Renal Failure patients
• All cases so far are associated with subjects who
  have renal failure.
• Not all subjects with Chronic Kidney Disease
  (CKD) are at risk. Those with lower kidney
  function (esp. those on dialysis) are at higher
  risk, it seems.
• A cutoff of GFR lt30mL/min (CKD Stage 4) is
  currently held by the FDA as a cutoff for high
  risk designation (or Crgt1.5)
• ANY case of acute renal failure is a
  contraindication for use of Gd contrast agents
  (a transiently low or quickly worsening renal
  function, that is).

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Who is at risk?

• Additional Factors
• Renal patients read CKD who have recently had a
  vascular manipulation (fistula placement for
  example)
• Renal patients who have recently had a DVT, PE,
  thrombosis, or who are hypercoagulable (Factor V
  Leiden deficiency, etc.)
• Renal patients who are on very high doses of
  Aranesp/Epo

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Nephrogenic fibrosing dermopathy
Huh?

• What the heck is this?

How does it occur?
Who is at risk?
Is it serious?
Who needs to know about it?
Is there a treatment for it?
What are the options?
Review
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Is it serious?
In some cases, NSF leads to serious physical
disability including wheelchair requirement. it
is now known that several organs such as liver,
lungs, muscles and heart may be involved. Organ
involvement may explain the suspected increased
mortality of patients with NSF. There is no
established treatment for NSF, Severely
affected patients may be unable to walk, or fully
extend the joints of their arms, hands, legs, and
feet. Complaints of muscle weakness are common.
Approximately 5 of patients have a rapidly
progressive (fulminant) course.
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Nephrogenic fibrosing dermopathy
Huh?

• What the heck is this?

How does it occur?
Who is at risk?
Is it serious?
Who needs to know about it?
Is there a treatment for it?
What are the options?
Review
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Who needs to know about it?

• Radiologists
• Nephrologists

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Who needs to know about it?

• Radiologists
• Nephrologists
• Nephrology staff members
• Primary Care providers
• Primary Care staff members

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Who needs to know about it?

• Radiologists
• Radiology Technicians and staff
• Nephrologists
• Nephrology staff members
• Dialysis nursing staff
• Primary Care providers
• Primary Care staff members

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Nephrogenic fibrosing dermopathy
Huh?

• What the heck is this?

How does it occur?
Who is at risk?
Is it serious?
Who needs to know about it?
Is there a treatment for it?
What are the options?
Review
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Is there a treatment for it?
49
Is there a treatment for it?

• Immune globulin (IgG)

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Is there a treatment for it?

• Immune globulin (IgG)
• Unproven case series small

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Is there a treatment for it?

• Immune globulin (IgG)
• Plasmapheresis

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Is there a treatment for it?

• Immune globulin (IgG)
• Plasmapheresis
• Unproven likely no help

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Is there a treatment for it?

• Immune globulin (IgG)
• Plasmapheresis
• Steroids with chemo (cytoxan, et al)

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Is there a treatment for it?

• Immune globulin (IgG)
• Plasmapheresis
• Steroids with chemo (cytoxan, et al)
• Failure

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Is there a treatment for it?

• Immune globulin (IgG)
• Plasmapheresis
• Steroids with chemo (cytoxan, et al)
• Ultraviolet (UVA) therapy

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Is there a treatment for it?

• Immune globulin (IgG)
• Plasmapheresis
• Steroids with chemo (cytoxan, et al)
• Ultraviolet (UVA) therapy
• Unproven no profound benefit so far

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Is there a treatment for it?

• Immune globulin (IgG)
• Plasmapheresis
• Steroids with chemo (cytoxan, et al)
• Ultraviolet (UVA) therapy
• Extracorporeal Photopheresis (huh?)

58
Is there a treatment for it?

• Immune globulin (IgG)
• Plasmapheresis
• Steroids with chemo (cytoxan, et al)
• Ultraviolet (UVA) therapy
• Extracorporeal Photopheresis (huh?)
• Removal of blood and exposing it to
  photoactivated chemotherapy then reinfusing the
  blood
• Unproven - possible benefit

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Is there a treatment for it?

• Immune globulin (IgG)
• Plasmapheresis
• Steroids with chemo (cytoxan, et al)
• Ultraviolet (UVA) therapy
• Extracorporeal Photopheresis (huh?)
• Renal Transplantation

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Is there a treatment for it?

• Immune globulin (IgG)
• Plasmapheresis
• Steroids with chemo (cytoxan, et al)
• Ultraviolet (UVA) therapy
• Extracorporeal Photopheresis (huh?)
• Renal Transplantation
• Unproven probable benefit

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Is there a treatment for it?

• Immune globulin (IgG)
• Plasmapheresis
• Steroids with chemo (cytoxan, et al)
• Ultraviolet (UVA) therapy
• Extracorporeal Photopheresis (huh?)
• Renal Transplantation
• Resumption of normal renal function
• Successful obviously rare in all but acute
  failure cases

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Is there a treatment for it?

• Immune globulin (IgG)
• Plasmapheresis
• Steroids with chemo (cytoxan, et al)
• Ultraviolet (UVA) therapy
• Extracorporeal Photopheresis (huh?)
• Renal Transplantation
• Resumption of normal renal function
• In summary no proven treatment exists except
  for the resumption of normal renal function
  which in chronic renal failure patients is only
  available by way of transplantation.

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Nephrogenic fibrosing dermopathy
Huh?

• What the heck is this?

How does it occur?
Who is at risk?
Is it serious?
Who needs to know about it?
Is there a treatment for it?
What are the options?
Review
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What are the options?

• Avoid at all costs
• No limitations
• No limitations (except in cases of heightened
  risk)
• Avoid Gd contrast and use other agents if
  unavoidable, see below
• These patients are usually on or will be starting
  hemodialysis placement of hemodialysis access
  (temporary or permanent) and initiation of
  dialysis directly after contrast load is
  acceptable

• Acute Renal Failure
• GFR gt60mL/min CKD Stage 2 or 1
• GFR gt30mL/min lt60mL/min CKD Stage 3
• GFR gt15mL/min lt30mL/min
• CKD Stage 4
• GFR lt15mL/min
• CKD Stage 5 (ESRD)

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Nephrogenic fibrosing dermopathy
Huh?

• What the heck is this?

How does it occur?
Who is at risk?
Is it serious?
Who needs to know about it?
Is there a treatment for it?
What are the options?
Review
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Review
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Nephrogenic Systemic Fibrosis

• IS
• only found in patients with moderate to severe
  renal impairment

• IS NOT
• Found in patients without renal failure

There are no reports of NSF in patients with
normal kidney function. Around 200 million
patients have had injections of
a gadolinium-based contrast agent since the early
1980s. A population of more than 30 million
patients has received gadodiamide. So, in
patients without ESRD, all gadolinium-based
contrast agents seem to be safe. 5 Most cases
reported involve patients with a GFR of lt20mL/min
(ESRD is defined at lt15mL/min).
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Nephrogenic Systemic Fibrosis

• IS
• Found in patients who have NOT received Gd
  contrast agents

• IS NOT
• Usually seen outside of cases related to
  Gadolinium (Gd) contrast agents

Several NSF cases reported by Marckmann were
exposed to gadodiamide earlier without developing
signs of NSF. This observation suggests that
gadodiamide was a necessary, but not a sufficient
cause of NSF. Certain other factors must have
played a role, but they were not able to identify
any such cofactor. Also, the fact that NSF can
develop in patients in whom it cannot be
documented that they have had a gadolinium-based
agent speaks in favor of a cofactor. 5
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Nephrogenic Systemic Fibrosis

• IS
• Proven to affect the skin, vasculature, and
  internal organs
• Found to occur between 2 days and 18 months after
  Gd exposure

• IS NOT
• Limited to skin involvement
• Only acute in nature though most cases occur
  within one month of contrast load

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Nephrogenic Systemic Fibrosis

• IS
• Seen in patients already on dialysis
• Almost exclusively seen in patients exposed to
  Gadodiamide (Omniscan)

• IS NOT
• Directly caused by dialysis
• Only found in patients on dialysis
• - Thought to be seen in patients receiving other
  types of Gd contrast, but the FDA has ruled
  other agents as high risk as well

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Nephrogenic Systemic Fibrosis

• IS
• A new disease
• Debilitating and deadly
• Avoidable

• IS NOT
• Curable
• Curable
• Curable

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HTN
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Hypertension

• New Treatment Options.

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Hypertension New treatment options 18

• Defining hypertension

78
Hypertension New treatment options

• Defining hypertension
• Pressures gt140/90? (Screening)

79
Hypertension New treatment options

• Defining hypertension
• Pressures gt140/90?
• Pressures gt130/80? (Diabetics, CKD)

80
Hypertension New treatment options

• Defining hypertension
• Pressures gt140/90?
• Pressures gt130/80? (Diabetics, CKD)
• Pressures gt120/80? (Optimal/Normal)

81
Hypertension New treatment options

• Defining hypertension
• Pressures gt140/90?
• Pressures gt130/80? (Diabetics, CKD)
• Pressures gt120/80? (Optimal/Normal)
• Pressures gt115 systolic? (statistical increase in
  cardiac risk)

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Hypertension New treatment options

• Defining hypertension
• Pressures gt140/90?
• Pressures gt130/80? (Diabetics, CKD, and CAD)
• Pressures gt120/80? (Optimal)
• Pressures gt115 systolic? (statistical increase in
  cardiac risk)

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Hypertension New treatment options

• Defining hypertension
• Measuring hypertension

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Hypertension New treatment options

• Defining hypertension
• Measuring hypertension
• Office measurements vs.. home measurements 19

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Hypertension New treatment options

• Defining hypertension
• Measuring hypertension
• Office measurements vs. home measurements 19
• Ambulatory measurements when? 20

86
Hypertension New treatment options

• Defining hypertension
• Measuring hypertension
• Office measurements vs. home measurements 19
• Ambulatory measurements when? 20
• Pulse wave velocity measurement 21

87
Hypertension New treatment options

• Defining hypertension
• Measuring hypertension
• Hypertension and the Kidney

88
Hypertension New treatment options

• Defining hypertension
• Measuring hypertension
• Hypertension and the Kidney
• Aldosterone
• Renin
• Uric Acid
• Vitamin D
• Renal Artery Stenosis (Renovascular hypertension)

89
Hypertension New treatment options

• Defining hypertension
• Measuring hypertension
• Hypertension and the Kidney
• Treatment of hypertension

90
Hypertension New treatment options

• Defining hypertension
• Measuring hypertension
• Hypertension and the Kidney
• Treatment of hypertension

91
Hypertension New treatment options

• Something old
• Something new
• Something used
• Something blue

92
Hypertension New treatment options

• Something old
• B-blockers
• Chlorthalidone
• Something new
• Aliskiren (Tekturna)
• Something borrowed
• ACEIs and ARBs
• Something blue
• Nebivolol (Bystolic)

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B-Blockers

• ASCOT (Anglo-Scandinavian Cardiac Outcome Trial)
• LIFE (Losartan Intervention for Endpoints)
• These trials show poorer outcomes in endpoints
  for B-blockers versus all other agents when used
  as first line agents for blood pressure control
  (CV mortality, all-cause mortality, Stroke, new
  dx of diabetes) cardioprotective effects are
  still significant, though.

95
B-Blockers

• ASCOT (Anglo-Scandinavian Cardiac Outcome Trial)
• LIFE (Losartan Intervention for Endpoints)
• the British Hypertension Society has removed
  B-blockers from its treatment algorithm for
  primary uncomplicated hypertension. 18

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Chlorthalidone

• Hygroton (Chlorthalidone) is a thiazide diuretic
  similar to HCTZ recently used in the Systolic
  Hypertension in the Elderly Program (SHEP) as
  well as other trials.

98
Chlorthalidone

• Hygroton (Chlorthalidone) is a thiazide diuretic
  similar to HCTZ recently used in the Systolic
  Hypertension in the Elderly Program (SHEP) as
  well as other trials.
• Compared to HCTZ its BP lowering effect is
  similarly efficacious

99
Chlorthalidone

• Hygroton (Chlorthalidone) is a thiazide diuretic
  similar to HCTZ recently used in the Systolic
  Hypertension in the Elderly Program (SHEP) as
  well as other trials.
• Compared to HCTZ its BP lowering effect is
  similarly efficacious
• Nocturnal BP control was significantly improved
  from HCTZ (n30). 26

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Aliskiren

• Tekturna from Novartis

102
Aliskiren

• Tekturna from Novartis
• Why not sooner?

103
Aliskiren

• Tekturna from Novartis
• Why not sooner? Bioavailability (2.5)

104
Aliskiren

• Tekturna from Novartis
• Why not sooner?
• What is it?

105
Aliskiren

• is an orally active, nonpeptide, potent renin
  inhibitor. per the FDA prescribing information
  insert

106
Aliskiren

• Tekturna from Novartis
• Why not sooner?
• What is it?
• How does it work?

107
Aliskiren 20
108
Aliskiren 14
109
Aliskiren

• Tekturna from Novartis
• Why not sooner?
• What is it?
• How does it work?
• How WELL does it work? 21,22
• Systolic BP drops 10-20 mmHg
• Diastolic BP drops 5-20 mmHg

110
Aliskiren

• Tekturna from Novartis
• Why not sooner?
• What is it?
• How does it work?
• How WELL does it work?
• Systolic BP drops 15-20 mmHg
• Diastolic BP drops 5-20 mmHg
• In combination with other antihypertensives, an
  additional 5-10 mmHg drop can be expected in many
  cases

111
Aliskiren

• Tekturna from Novartis
• Why not sooner?
• What is it?
• How does it work?
• How WELL does it work?
• Side effects?

112
Aliskiren

• Tekturna from Novartis
• Why not sooner?
• What is it?
• How does it work?
• How WELL does it work?
• Side effects?
• Similar to other RAAS blockade agents
• Hyperkalemia, Hypotension, Angioedema, Cough (50
  of the incidence of ACE-inhibitors),
  Hyperuricemia, Teratogenic effects

113
Aliskiren

• Tekturna from Novartis
• Why not sooner?
• What is it?
• How does it work?
• How WELL does it work?
• Side effects?
• So is it worth using?

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115
ACEi and ARB

• Distinctions between ACEi and ARB therapy are
  becoming smaller and smaller

116
ACEi and ARB

• Distinctions between ACEi and ARB therapy are
  becoming smaller and smaller
• ACEi and ARB therapy were not significantly
  different in their effect on death,
  cardiovascular events, lipid levels, progression
  to diabetes (i.e. metabolic effect), LV mass, or
  renal disease. 27

117
ACEi and ARB

• Distinctions between ACEi and ARB therapy are
  becoming smaller and smaller
• ACEi and ARB therapy were not significantly
  different in their effect on death,
  cardiovascular events, lipid levels, progression
  to diabetes (i.e. metabolic effect), LV mass, or
  renal disease. 27
• ACEi and ARB therapy is equal when compared for
  proteinuria control together they are even
  better
• Of note here no trials for adverse effect
  increases have been made to date all trials
  have been fairly short 28

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119
Nebivolol
                                 

                                 

• Bystolic from Mylan Laboratories and Forest
  Laboratories
• B1-selective antagonist (with B2 activity in high
  doses)

120
Nebivolol15

• Bystolic from Mylan Laboratories and Forest
  Laboratories
• B1-selective antagonist (with B2 activity in high
  doses)
• Reportedly less Erectile Dysfunction, less
  problematic airway symptoms (e.g., asthma
  exacerbations B2 effects), less fatigue, less
  alteration of insulin, glucose, and lipid levels
• Nitric Oxide production (B3 stimulation?) which
  leads to further vasodilatation
  L-arginine/nitric oxide pathway

121
Nebivolol15

• Bystolic from Mylan Laboratories and Forest
  Laboratories
• B1-selective antagonist (with B2 activity in high
  doses)
• Reportedly less Erectile Dysfunction, less
  problematic airway symptoms (e.g., asthma
  exacerbations B2 effects), less fatigue, less
  alteration of insulin, glucose, and lipid levels
• Nitric Oxide production (B3 stimulation?) which
  leads to further vasodilatation
  L-arginine/nitric oxide pathway
• The new Viagra ?

122
Nebivolol15

• Bystolic from Mylan Laboratories and Forest
  Laboratories
• B1-selective antagonist (with B2 activity in high
  doses)
• Is it worth using?

123
Nebivolol15

• Bystolic from Mylan Laboratories and Forest
  Laboratories
• B1-selective antagonist (with B2 activity in high
  doses)
• Is it worth using?
• As effective at BP control 23
• Improved coronary flow vs.. atenolol in one study
  24
• Possible improved overall efficacy in patients
  with decreased vascular compliance (NO-pathway
  vasodilatory effects) 25

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125
BICARB
126
Sodium Bicarbonate

• Radiocontrast Nephropathy Made Worse?

127
Sodium Bicarb and ConNeph

• Old wisdom and new studies have shown some
  preference for hydration and, in some cases
  hydration with alkali to prevent contrast
  nephropathy.

128
Sodium Bicarb and ConNeph

• Old wisdom and new studies have shown some
  preference for hydration and, in some cases
  hydration with alkali to prevent contrast
  nephropathy. (Below is Merten, et al)
• The primary end point of contrast-induced
  nephropathy occurred in 8 patients (13.6)
  infused with sodium chloride but in only 1 (1.7)
  of those receiving sodium bicarbonate (mean
  difference, 11.9 95 confidence interval CI,
  2.6-21.2 P .02) n119. 29

129
Sodium Bicarb and ConNeph

• New evidence? (From et al, below)
• After adjustment for total volume of hydration,
  medications, age, gender, prior creatinine,
  contrast iodine load, prior exposure to contrast
  material, type of imaging study, heart failure,
  hypertension, renal failure, multiple myeloma,
  and diabetes mellitus, use of sodium bicarbonate
  alone was associated with an increased risk of
  contrast nephropathy compared with no treatment
  (odds ratio 3.10, 95 confidence interval 2.28 to
  4.18 P lt 0.001) n11,516. 30

130
Sodium Bicarb and ConNeph

• New evidence? (From et al, below)
• N-AC with or without NaHCO3 did not change
  outcomes

131
Sodium Bicarb and ConNeph

• New evidence? (From et al, below)
• Difference ?
• Merten, et al A prospective, single-center,
  randomized trial
• From, et al retrospective, single-center
  analysis

132
Sodium Bicarb and ConNeph

• New evidence? (From et al, below)
• Difference ?
• Multiple trials including bicarbonate have been
  performed, many showing some benefit with the
  alkalimore studies will need to be done

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134
EGFR
135
eGFR

• When and How to Use It.

136
eGFR

• estimated Glomerular Filtration Rate
• GFR Substance xu x Urinary Flow Rate
• Substance xp

137
eGFR

• estimated Glomerular Filtration Rate
• GFR Substance xu x Urinary Flow Rate
• Substance xp
• eCrCl (140-Age) x Mass(kg) x 0.85 (if female)
• 72 x Serum Creatinine (mg/dL)

138
eGFR

• estimated Glomerular Filtration Rate
• GFR Substance xu x Urinary Flow Rate
• Substance xp
• eCrCl (140-Age) x Mass(kg) x 0.85 (if female)
• 72 x Serum Creatinine (mg/dL)
• eGFR 170 x sCr-0.999 x age-0.176 x BUN-.170 x
  Albumin0.318
• (x 0.762 if female) (x 1.180 if black)

139
eGFR

• estimated Glomerular Filtration Rate
• eGFR 170 x sCr-0.999 x age-0.176 x BUN-.170 x
  Albumin0.318
• (x 0.762 if female) (x 1.180 if black)

140
eGFR

• Values are not normalized for BSA.
• Values are usually listed separately for African
  Americans and non-African Americans.
• Values are more inaccurate for eGFRs that
  approach normal levels.
• Values consistently overestimate true GFRs for
  patients that have severely decreased GFRs.

141
eGFR

• When
• the pt is at his/her assumed baseline renal
  function.
• the patient is aged (gt60 yo).
• the patient has known advanced CKD.

142
eGFR

• When
• the pt is at his/her assumed baseline renal
  function.
• the patient is aged (gt60 yo).
• the patient has known advanced CKD.
• How
• as a backup estimate to your own.
• to estimate TtD (time to dialysis).
• to help determine the time for consultation.

143
eGFR

• Ok, I dont have an eGFR available to me.

144
eGFR

• Ok, I dont have an eGFR available to me.
• When 1 is not 1

145
eGFR

• Ok, I dont have an eGFR available to me.
• When 1 is not 1
• Baseline 1.0

146
eGFR

• Ok, I dont have an eGFR available to me.
• When 1 is not 1
• Baseline 1.0
• Subtract 0.1 if female, gt65 yo, small-framed
• Subtract 0.3 if physically debilitated or
  cachectic
• Add 0.1 if muscular or if fit and gt200 lbs.
• Add 0.2 if plays professional football

147
eGFR

• Ok, I dont have an eGFR available to me.
• When 1 is not 1
• Baseline 1.0
• Subtract 0.1 if female, gt65 yo, small-framed
• Subtract 0.2 if physically debilitated or
  cachectic
• Add 0.1 if muscular or if fit and gt200 lbs.
• Add 0.2 if plays professional football
• My pt. is a 72 yo white female who is 50 her
  Cr is 1.4 mg/dL today.

148
eGFR

• Ok, I dont have an eGFR available to me.
• When 1 is not 1
• Baseline 1.0
• Subtract 0.1 if female, gt65 yo, small-framed
• Subtract 0.2 if physically debilitated or
  cachectic
• Add 0.1 if muscular or if fit and gt200 lbs.
• Add 0.2 if plays professional football
• 1.0 0.1(female) -0.1(gt65yo) -0.1(small) 0.7
• Divide the result by the current Cr (0.7 / 1.4
  0.5)
• In this case the eGFR is 50 normal and CrCl is
  35-45 mL/min.

149
eGFR

• CKD Staging
• Stage 1 GFR gt 90mL/min
• Stage 2 GFR gt60 and lt90mL/min
• Stage 3 GFR gt30 and lt60mL/min
• Stage 4 GFR gt15 and lt45mL/min
• Stage 5 GFR lt15mL/min

150
eGFR

• CKD Staging
• Stage 1 GFR gt 90mL/min
• Stage 2 GFR gt60 and lt90mL/min
• Stage 3 GFR gt30 and lt60mL/min
• Stage 4 GFR gt15 and lt45mL/min
• Stage 5 GFR lt15mL/min

151
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152
Refreshment time
153
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154
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